All based on the same work. Sounds like a real connection was made in this new work showing a link between bad dental hygiene and Alzheimer's, and also between the bacterium Porphyromonas gingivalis and Alzheimer's. These would both be a big big deal. After all - tooth decay is something you can do something about. And if tooth decay causes Alzheimer's - then - well - we could probably prevent Alzheimer's.

Hmm .. that is weird. The paper does not seem to have anything in it really closely tied to all the claims in the news stories. Here is the Abstract:

The aim of this study was to establish a link between periodontal disease and Alzheimer's disease (AD) with a view to identifying the major periodontal disease bacteria (Treponema denticola, Tannerella forsythia, and Porphyromonas gingivalis) and/or bacterial components in brain tissue from 12 h postmortem delay. Our request matched 10 AD cases for tissue from Brains for Dementia Research alongside 10 non-AD age-related controls with similar or greater postmortem interval. We exposed SVGp12, an astrocyte cell line, to culture supernatant containing lipopolysaccharide (LPS) from the putative periodontal bacteria P. gingivalis. The challenged SVGp12 cells and cryosections from AD and control brains were immunolabeled and immunoblotted using a battery of antibodies including the anti-P. gingivalis-specific monoclonal antibody. Immunofluorescence labeling demonstrated the SVGp12 cell line was able to adsorb LPS from culture supernatant on its surface membrane; similar labeling was observed in four out of 10 AD cases. Immunoblotting demonstrated bands corresponding to LPS from P. gingivalis in the SVGp12 cell lysate and in the same four AD brain specimens which were positive when screened by immunofluorescence. All controls remained negative throughout while the same four cases were consistently positive for P. gingivalis LPS (p = 0.029). This study confirms that LPS from periodontal bacteria can access the AD brain during life as labeling in the corresponding controls, with equivalent/longer postmortem interval, was absent. Demonstration of a known chronic oral-pathogen-related virulence factor reaching the human brains suggests an inflammatory role in the existing AD pathology.

Alas, even via UC Davis Libraries I do not have access to the full article. So my inferences will have to be based on the abstract (note to authors, if you want people to judge your full papers not just your abstracts, well, it would be good to have your paper be available). From what I can tell - what they showed in this paper is that antibodies that are known to find to lipopolysaccharide (LPS) from P. gingivalis showed positive binding to brain material from a few patients who had Alzheimer's and did not show binding to brain material from controls. So let's ask and try to answer a few questions about this:

Does LPS from a specific organism in the brain mean that the organism was in the brain: I don't think so - LPS could move around?

Does binding by the antibody they used mean that there is LPS from P. gingivalis there? Definitely no - there could be cross reactivity with other LPSs or even other molecules?

Did they do any more specific tests (e.g., DNA)? Doesn't seem like it.

But let us just assume that they really did detect P. gingivalis in the brains of Alzheimer's patients. Would this mean PG causes Alzheimer's? Obviously it does not mean that. Let us even assume (ridiculously) that PG causes Alzheimer's. Would this mean the periodontal disease leads to Alzheimer's? No - PG could come into brains in other ways.

I could go on and on. There are so so so so so so so many jumps that are needed to go from the limited results presented in this paper to getting anywhere near supporting a hypothesis that periodontal disease causes Alzheimer's that it makes we want to scream. The news reporting here is awful. The scientists involved seem to be overhyping their work to extremes with risky, dangerous possible consequences (e.g., - oh - so you have Alzheimer's - it's your fault for not taking care of your teeth ... we need more money for dental care to prevent Alzheimer's; everyone should take prophylactic antibiotics to prevent Alzheimer's and so on).

"At rOpenSci we are creating packages that allow access to data repositories through the R statistical programming environment that is already a familiar part of the workflow of many scientists. We hope that our tools will not only facilitate drawing data into an environment where it can readily be manipulated, but also one in which those analyses and methods can be easily shared, replicated, and extended by other researchers. While all the pieces for connecting researchers with these data sources exist as disparate entities, our efforts will provide a unified framework that will be quickly connect researchers to open data."

A major new technology has been developed by The University of Nottingham, which enables all of the world's crops to take nitrogen from the air rather than expensive and environmentally damaging fertilisers

And

This ground-breaking development potentially provides every cell in the plant with the ability to fix atmospheric nitrogen. The implications for agriculture are enormous as this new technology can provide much of the plant's nitrogen needs.

And

Applied to the cells of plants (intra-cellular) via the seed, it provides every cell in the plant with the ability to fix nitrogen. Plant seeds are coated with these bacteria in order to create a symbiotic, mutually beneficial relationship and naturally produce nitrogen.

And

N-Fix is a natural nitrogen seed coating that provides a sustainable solution to fertiliser overuse and Nitrogen pollution. It is environmentally friendly and can be applied to all crops. Over the last 10 years, The University of Nottingham has conducted a series of extensive research programmes which have established proof of principal of the technology in the laboratory, growth rooms and glasshouses.

And

There is a substantial global market for the N-Fix technology, as it can be applied globally to all crops. N-Fix has the power to transform agriculture, while at the same time offering a significant cost benefit to the grower through the savings that they will make in the reduced costs of fertilisers. It is a great example of how University research can have a world-changing impact.

And

The proof of concept has already been demonstrated. The uptake and fixation of nitrogen in a range of crop species has been proven to work in the laboratory and Azotic is now working on field trials in order to produce robust efficacy data. This will be followed by seeking regulatory approval for N-Fix initially in the UK, Europe, USA, Canada and Brazil, with more countries to follow.

Sounds f$*@#$# awesome. So awesome that it was picked up by multiple news sources including

The only problem is - they don't present any evidence. None. No data. No paper. No poster. Nothing. It is simply a press release with a bunch of words. Ridiculous. I think I am going to announce I have a way to not only get all crops to fix nitrogen, but that it will work by telepathy. This is one of the worst science-by-press-release cases I have ever ever seen.

7/26/13

Postdoc Position in Innovating Scholarly Communication

A new UC Davis initiative on "Innovating the Communication of Scholarship" is hiring a 3-year postdoctoral fellow, starting September 1, 2013. This is a cross-disciplinary project to study the future of academic publishing, involving faculty from the Center for Science and Innovation Studies, the Library, the Genome Center, and the School of Law (with additional collaborators in Computer Science, English, Philosophy, and the Graduate School of Management). Research topics include open access models, peer review, new forms of quality metrics, data publication, use of social media, and new forms of misconduct.

The successful candidate will conduct research, collaborate on or lead organization of conferences, workshops, pedagogical activities, and grant writing. A Ph.D. is required in a relevant field such as Science and Technology Studies, Library and Information Sciences, Communication, Law, Science, or English. Other disciplines will be considered depending on the specific focus of the candidate?s research and other experience. Qualified applicants will have experience working successfully in teams and managing multi-year projects. He or she will possess excellent written and oral communication and administrative skills.

Salary is based on experience and qualifications according to UC Davis guidelines.

Another quick post. Just read this article in LiveScience about a new PLOS One paper: Condoms May Boost Beneficial Vaginal Bacteria | LiveScience. Am wondering - when will condoms start coming with probiotics in them? Anyone out there know if this has been done yet? I mean, I do not want to oversell the microbiome but hey it seems like there could be something to do here ...

UPDATE 10 minutes later - not saying I endorse or support everything Suber says (I am much more enthusiastic about gold open access than green OA which I find limited in use). But the interview is worth a read.

The rapid advance in genetic sequencing technologies has provided an unprecedented amount of data on the biodiversity of meiofauna. It was hoped that these data would allow the identification and counting of species, distinguished as tight clusters of similar genomes. Surprisingly, this appears not to be the case. Here, we begin a theoretical discussion of this phenomenon, drawing on an individual-based ecological model to inform our arguments. The determining factor in the emergence (or not) of distinguishable genetic clusters in the model is the product of population size with mutation rate—a measure of the adaptability of the population as a whole. This result suggests that indeed one should not expect to observe clearly distinguishable species groupings in data gathered from ultrasequencing of meiofauna.

I was pointed to it by Greg Pasternack from UC Davis who has been a major force in trying to guarantee academic freedoms at UC Davis.

Colleagues,

Four years and one month after the UCD Committee on Academic Freedom and Responsibility first raise the alarm about the danger of unjust discipline faculty in the UC system may face (and certainty have faced) for speech and actions regarding institutional matters, I am very happy to report to you all that on July 18 the UC Regents approved our proposed amendment to APM-015 that guarantees faculty academic freedom to speak out about institutional matters. Given the number of judges that have ruled that faculty speech on institutional matters is *not* protected by the First Amendment, even in public universities, getting this freedom inscribed into APM-015 provides a policy-based guarantee no longer reliant on external interpretation.

This is the greatest expansion in academic freedom in the history of the UC system, because all previous notions of academic freedom limited the application of the idea to just one's area of scholarship. Prior to this, the biggest change was to no longer require "dispassionate" scholarship. However, academic freedom is no longer shackled to scholarship. We are free to speak on all institutional matters, whether they are within our sphere of scholarship or not. We may do so using any forum or medium.

Now go out and use your freedom to stir up brilliant controversies ;)

Best wishes,

-Prof. Greg Pasternack

The section he called particular attention to is in line 4 in the part on "Professional Rights of Faculty" which reads "freedom to address any matter of institutional policy or action when acting as a member of the faculty whether or not as a member of an agency of institutional governance." This clearly relates to some real and perceived challenges to academic freedom at various UCs and it is good to have a formal policy that says such a freedom is a right of the faculty.

Friday, July 19, 2013

Guest Post by Joshua Weitz, Associate Professor, School of Biology and School of Physics, Georgia Institute of Technology

Introduction

I direct a theoretical ecology and quantitative biology group based in the School of Biology at Georgia Tech.I am going on a 9 month “leave” (Georgia Tech does not call them sabbaticals) to the Department of Ecology and Evolutionary Biology at the U of Arizona in Tucson, AZ from August 2013-May 2014 where I will be based in Matthew Sullivan’s Tucson Marine Phage Laboratory.In preparation for this leave, our group held an interactive discussion on challenges and opportunities arising from the PI sabbatical for faculty, postdocs and PhD students in the sciences.The discussion took place in four parts in a one-hour period.Below I describe the setup of the discussion followed by specific recommendations for faculty, postdocs and PhD students prior to the PI sabbatical.

How to Talk about the PI Sabbatical

Part 1 – the setup: I asked for a show of hands of group members who had thought about how my sabbatical would change the group and its dynamics?Nearly all members raised their hands.When asked, the group members also noted that they were most concerned about how the sabbatical would affect them.Hence, in an effort to try and understand the effect of the sabbatical on all members, we split into three small discussion groups which were asked to identify challenges and opportunities for (i) the PI; (ii) postdocs; (iii) PhD students.

Part 2 – small group discussion: The individual groups talked about how the sabbatical would affect different group members.There are currently 9 members in the group (not including the PI), so we divided into three groups of three (I did not actively participate in the small group discussions, but did check in on all three groups).The PI group was comprised of one postdoc, 1 graduate and 1 undergraduate.The postdoc group had 1 postdoc and 2 graduate students.The grad student group had 3 graduate students. Hence, the first item of discussion was an effort to identify issues at stake at each career stage.Then, the groups began to discuss how the sabbatical might change business as usual.The groups spoke for ~15 minutes.

Part 3 - reporting: Challenges and opportunities were identified for each of the three categories.A number of salient themes emerged that serve as general recommendations.The consensus was that a number of common themes would emerge prior to a sabbatical although each science research group may differ in its own interactions.Our presumption is that the PI was going alone and this shaped the nature of our recommendations.First, as suggested by one of the students, there was a sense that the PI sabbatical would lead the students into a “Spiderman situation” in the sense that “with great power comes great responsibility”.The PI sabbatical would lead to greater independence for group members and that this independence involves greater need for self-motivation, taking a holistic (long-term) view of one’s research, and increased pre-planning given the changes to the PI’s availability.Second, clear communication is essential. For example, if a PI plans to be incommunicado for long stretches of time, this may be manageable (even if non-ideal from a student perspective), so long as provisions have been made to handle both the administrative and research duties that the PI normally would handle.As a rule of thumb, the greater the change in PI availability, the greater the need for pre-planning to ensure that students and postdocs remain on track for research, career and personal development goals.

Part 4 – the view of the PI: I provided additional feedback, tailored to the group and specifically addressed an issue that could create the most anxiety: my availability for one-on-one interactions.I also distributed an initial recommendation list, modified here in light of group discussion.

Thursday, July 18, 2013

Just finally getting notes up from the SMBE 2013 meeting session on "Diversity and evolution of microbes and their genomes" that I chaired. After some issues with Storify I managed to record a "storification" with Twitter posts from the session. It is embedded below.

The talks were as follows:
Invited Talks

Holly Bik, UC Davis, Microbial Metazoa and the Taxonomic Abyss

Lauras Katz, Smith College, Genome Dynamics across the Eukaryotic Tree of Life

Jennifer Gardy, Of Snow and Short Reads: How Microbial Genomics Is Changing Public Health, British Columbia Center for Disease Control

Quick post here. This paper came out a few months ago but it was not freely available so I did not write about it until now as it just showed up in Pubmed Central. It was published in the Journal of Bacteriology but they do not release material for free onto their website or Pubmed Central for a few months. Alas, as I was kind of a peripheral player in the main work in the paper (I helped them with the phylogenetic profiling part) I did not end up pushing as hard as I should have for paying the open access fee to make it available earlier / openly.

And in that paper we did a phylogenetic profile based analysis of sporulation genes and found a set of genes that were (on average) in all the sporulating species and not in non sporulating species. Among this set of genes were quite a few that nobody had ever shown to be involved in sporulation. We predicted that they were likely involved in sporulation.

And then I waited, since I did not really work on sporulation. And in a series of discussions with Losick and people in his lab found out that they had evidence that many of these genes in B. subtilis were involved in sporulation. And the latest paper is in essence a follow up on some of those discussions (well, really it is a lot of work from Losick's lab with a little input from those conversations to guide some of the experimental tests).

Wednesday, July 17, 2013

Quick post here. This paper came out a few months ago but it was not freely available so I did not write about it (it is in PNAS but was not published with the PNAS Open Option — not my choice – lead author did not choose that option and I was not really in the loop when that choice was made).

Anyway – it is now in Pubmed Central and at least freely available so I felt OK posting about it now. It is in a way a follow up to the “A phylogeny driven genomic encyclopedia of bacteria and archaea” paper (AKA GEBA) from 2009 with this paper a zooming in on the cyanobacteria.

Sunday, July 07, 2013

We went into the tunnel area (where you are in essence inside the big tank). And they announced they were having a shark feeding. We (11 of us including four kids) waited in the tunnel where they told us to.

The tunnel has a moving walkway in it on one side of the floor that slowly moves people through the area. On the other side of the floor there is solid ground. At the end of the walkway is a waiting area for the elevator. As the show started they turned on the walkway and people started moving past us. The walkway was wall to wall people.

As they turned on the walkway, the elevator could not keep up with the crowd pouring in off the walkway and it started to get very crowded there. We decided to try and get out because it felt unsafe in the tunnel. We squeezed onto the moving walkway (my wife first, with my two kids and then me).

Wednesday, July 03, 2013

Uggh. Just saw a bunch of stories about autism and the microbiome. Many of the comments in the news stories I read seemed, well, not so good. So I decided to sniff around. Seems that many of the comments and stories are based on a new PLOS One paper and the comments and press release from the group behind the paper.

In new research appearing in the journal PLOS ONE, a team led by Rosa Krajmalnik-Brown, a researcher at Arizona State University's Biodesign Institute, present the first comprehensive bacterial analysis focusing on commensal or beneficial bacteria in children with autism spectrum disorder (ASD).

This did not sound true and sounded a bit overblown as I could have sworn I had seen other "comprehensive" studies of the microbiome in children with ASD. So first I decided to look at the paper. And - thanks a lot - there was no link in the PR or the stories I had seen. So I had to go to PLOS One and do a little searching and I found it:

So - first I asked - did they make the same claim in the paper or was this just in the PR? Usually such things are just in the PR but amazingly they have this claim in the paper too, with lines like:

"previous studies describing the relationship between autism and gut microbes have either mostly focused on the emergence of harmful bacteria or mainly paid attention to already-known beneficial bacteria"

So I decided to then look at Pubmed and Google Scholar for other papers on autism and the microbiome. Here are some that I found:

Not all of these are what one would call comprehensive. But some of them are at least approaching the scale of what was done here. And surprisingly, not all of them are cited in the new study. In particular, the papers by Gondalia et al including one on "Molecular Characterisation of Gastrointestinal Microbiota of Children With Autism (With and Without Gastrointestinal Dysfunction) and Their Neurotypical Siblings" is not references despite it doing some similar things. I guess, if you don't cite other comparable studies, and pretend they don't exist, then that makes one's work seem a but more novel right? Weird not to cite that work though - not sure why that happened. And certainly some of the other studies, even though they are cited, seem like they could be referred to as comprehensive. I mean - Ian Lipkin's study did metagenomics not just PCR based sequencing. Isn't metagenomics sort of more comprehensive than PCR?

Anyway - let's just say this is not the first "comprehensive" study of autism and the microbome.

Moving on in the press release I encountered another painful statement.

The work also offers hope for new prevention and treatment methods for ASD itself, which has been on a mysterious and rapid ascent around the world.

Just what exactly does this new study say about prevention or treatment? Actually, as far as I can tell - nothing. So this is a bonus overselling statement just for the PR

Oh but then the PR just get's worse:

Their new study is the first to approach autism from a different angle, by examining the possible role of so-called commensal or beneficial bacteria.

Seriously? We have gone from trying to claim this is the first comprehensive study of the microbiome and autism to now saying it is the first? Fu#*(@@# ridiculous.

Other lines that are troubling are encountered further on including

"The authors stress that bacterial richness and diversity are essential for maintaining a robust and adaptable bacterial community capable of fighting off environmental challenges.". Hmm. What is the difference between richness and diversity? And what is the evidence that they are essential for such functions?

"The species is a common component in normal children exhibiting more diverse and robust microbial communities." Again - what makes that robust?

Michael Polan's recent New York Times Magazine story on the microbiome points to the fact that he is proud that his gut microbiome is rich in Prevotella regarding it as a possible sign of a healthy non-Western diet. Really? They brought Michael Pollan (with a mis-spelling that might be on purpose so that Pollan does not see this) into their PR? Uggh

Anyway - I kind of wanted to give them an overselling the microbiome award for some of their statements. But in the end I would rather give them an "Overselling ourselves" award. It is a shame too. I think continuing to explore possible connections between autism and the microbiome will be important. Making misleading statements about what you have done and not citing / properly referencing other work will not help.